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When levels are below 0.32 mmol/L (1.0 mg/dL) it is deemed to be severe. [2] Treatment depends on the underlying cause. [1] Phosphate may be given by mouth or by injection into a vein. [1] Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in the intensive care unit (ICU). [1] [3]
In critically ill patients admitted to an intensive care unit, if phosphate drops to below 0.65 mmol/L (2.0 mg/dL) from a previously normal level within three days of starting enteral or parenteral nutrition, caloric intake should be reduced to 480 kcals per day for at least two days while electrolytes are replaced. [3]
Common causes in pediatric patients may be diarrheal illness, frequent feedings with dilute formula, water intoxication via excessive consumption, and enemas. [3] Pseudohyponatremia is a false low sodium reading that can be caused by high levels of fats or proteins in the blood.
The complications of diabetes can dramatically impair quality of life and cause long-lasting disability. Overall, complications are far less common and less severe in people with well-controlled blood sugar levels. [3] [4] [5] Some non-modifiable risk factors such as age at diabetes onset, type of diabetes, gender, and genetics may influence risk.
The disorder is often accompanied by low calcium blood levels, which can result in muscle spasms. [1] Causes include kidney failure, pseudohypoparathyroidism, hypoparathyroidism, diabetic ketoacidosis, tumor lysis syndrome, and rhabdomyolysis. [1] Diagnosis is generally based on a blood phosphate level exceeding 1.46 mmol/L (4.5 mg/dL). [1]
Most neurons have the ability to use other fuels besides glucose (e.g. lactic acid, ketones).Knowledge of the "switchover" process is incomplete. [further explanation needed] The most severe neuroglycopenic symptoms occur with hypoglycemia caused by excess insulin because insulin reduces the availability of other fuels by suppressing ketogenesis and gluconeogenesis.